The effect of fasting, diet, and actinomycin D on insulin secretion in the rat.

The effect of fasting, diet, and actinomycin D on insulin secretion in the rat.
复制标题

禁食、饮食和放线菌素 D 对大鼠胰岛素分泌的影响。

DOI:
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发表时间:
1970
影响因子:
15.9
通讯作者:
D. Kipnis
D. Kipnis
中科院分区:
医学1区
文献类型:
--
作者:
N. Grey;S. Goldring;D. Kipnis

文献摘要

被引文献

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本研究旨在阐明空腹时葡萄糖刺激胰岛素分泌受损的机制。禁食48小时的大鼠在口服和静脉注射葡萄糖时胰岛素分泌反应均显示出明显的损伤。葡萄糖刺激的胰岛素分泌在24小时内恢复再喂养;放线菌素D再喂养前给予阻断正常的葡萄糖刺激的胰岛素分泌的预期回报,尽管足够的食物摄入。禁食大鼠再喂食缺乏碳水化合物的饮食未能显示正常的胰岛素分泌反应的回报,口服葡萄糖的大鼠喂等热量的高碳水化合物饮食。进食、禁食和禁食再喂食大鼠胰岛素分泌的差异不能归因于胰腺胰岛素含量的变化。有没有显着差异的胰岛素分泌反应,氨茶碱喂养,禁食,或禁食-再喂食大鼠。通过每8小时腹膜内注射少量葡萄糖(500 mg),间歇性脉冲禁食大鼠高血糖发作,改善了禁食状态下葡萄糖刺激的胰岛素分泌特征的损害。这些结果表明,葡萄糖刺激的胰岛素分泌在空腹和恢复再喂养过程中的损害是由胰腺β细胞中的葡萄糖诱导酶系统的变化调节。
The present studies were performed to elucidate the mechanisms responsible for the impairment of glucose-stimulated insulin secretion observed in fasting. Rats fasted for 48 hr displayed marked impairment in their insulin secretory response to both oral and intravenous glucose. Glucose-stimulated insulin secretion was restored within 24 hr by refeeding; actinomycin D given before refeeding blocked the expected return of normal glucose-stimulated insulin secretion despite adequate food intake. Fasted rats refed a diet devoid of carbohydrate failed to display a return of normal insulin secretory responsiveness to oral glucose in contrast to rats fed isocalorically a high carbohydrate diet. Differences in insulin secretion in fed, fasted, and fasted-refed rats could not be attributed to changes in pancreatic insulin content. There was no significant difference in the insulin secretory response to aminophylline of fed, fasted, or fasted-refed rats. The intermittent pulsing of fasted rats with hyperglycemic episodes by the injection of small amounts of glucose (500 mg) intraperitoneally every 8 hr ameliorated the impairment of glucose-stimulated insulin secretion characteristic of the fasting state. These results suggest that the impairment of glucose-stimulated insulin secretion during fasting and its restoration by refeeding are regulated by changes in a glucose-inducible enzyme system in the pancreatic beta cell.